Removal of the Fe(iii) site promotes activation of the human cystic fibrosis transmembrane conductance regulator by high-affinity Zn(ii) binding.

Abstract excerpt

The cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is activated by ATP binding at the interface of two cytoplasmic nucleotide binding domains (NBDs) and phosphorylation of the regulatory (R) domain by protein kinase A (PKA). The human CFTR has two functionally active thiol groups for gating regulation by chemical modification. Although modification of C832 in the R domain with...

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